MERYL COMER, Has Husband with Alzheimer’s Disease: It’s going to be good. Eat it for Harvey. Good job.

SUSAN DENTZER, NewsHour Health Correspondent: This is Harvey Gralnick, age 70, 12 years into the ravages of Alzheimer’s.

This was Harvey Gralnick at his prime. His diplomas and awards speak to his distinction as a longtime physician and research scientist at the National Institutes of Health. Gralnick was 58 at the peak of his NIH career when he was diagnosed with early-onset Alzheimer’s.

MERYL COMER: OK, good job.

SUSAN DENTZER: His wife, former television journalist Meryl Comer, describes how this main form of dementia sapped his intellect and destroyed his personhood.

MERYL COMER: Somebody once described it as a house where you see one light go off at a time, or watching somebody in slow motion die, lose their mind in front of your eyes, literally lose their mind in front of your eyes. Very painful to watch, especially knowing what he was.

Raising urgency to fight disease

SUSAN DENTZER: Comer, who's 62, now works with a team of nursing aides to care for her husband at home. She says her and her husband's story is a harbinger of things to come for her generation, the baby boom.

MERYL COMER: I want people to understand this disease, because it's going to be part of our future. It has the potential to be an epidemic in our generation, in the baby boom generation.

SUSAN DENTZER: So she's joined forces with a new group called ACT-AD, for Alzheimer's disease, to dramatically raise the sense of urgency to fight the condition. She spoke at a recent news conference.

MERYL COMER: I've come with another agenda that is shared in principle by everyone signing on to ACT-AD: the urgent need to change the conversation about this disease; accelerate the delivery of promising drugs to patients; improve the plight of families; and make this disease a national priority.

SUSAN DENTZER: An estimated 4.5 million Americans have Alzheimer's today, and the number is expected to triple within 10 years. The disease mainly strikes people in their 60s and beyond. By age 85, a stunning one-half of people have it.

MERYL COMER: Harv, can you see me? Harvey?

SUSAN DENTZER: But Gralnick's early-onset form mainly affects those in their 50s. Steve McConnell oversees policy and advocacy for the Alzheimer's Association.

STEPHEN MCCONNELL, Alzheimer's Association: We have found that as many as 600,000, somewhere between 200,000 and 600,000 baby boomers, people under age 65, have Alzheimer's disease, and that is truly terrifying.

SUSAN DENTZER: Early-onset Alzheimer's is traceable to genetic mutations passed down through families, but its symptoms are virtually identical to the form that hits other people later in life. Comer describes the first signs she saw in her husband.

Mystery behind the disease

SUSAN DENTZER: Comer says that, as she grew more concerned, she persuaded him to see a neurologist, who declared nothing amiss. Gralnick was later hospitalized for two months while doctors struggled to figure out what was wrong. Only later, as his symptoms worsened, did one venture the tentative diagnosis of Alzheimer's.

Dr. Sam Gandy is a leading neuroscientist at Thomas Jefferson University and chief scientific adviser to the Alzheimer's Association. He says scientists still don't fully understand what causes Alzheimer's disease and have several competing theories. Perhaps the leading one links the condition to changes in a common body protein, called amyloid.

DR. SAM GANDY, Thomas Jefferson University: Amyloid is actually normally made by all cells in the body all throughout life. In Alzheimer's disease, this protein changes its shape, becoming extremely sticky, forming clumps, and building up in between and outside of nerve cells.

SUSAN DENTZER: The amyloid proteins in Harvey Gralnick's brain had probably begun to change at least a decade before his symptoms became apparent. Gandy demonstrated how with a piece of wire.

DR. SAM GANDY: The process that begins Alzheimer's disease is what we call protein folding, and literally the amyloid protein folds back on itself like a big bobby-pin. And this then is a sticky form, and many of these bobby pin-like sticky structures aggregate together, clump together.

SUSAN DENTZER: Those sticky clumps of proteins are called amyloid plaques. For unknown reasons, they form only in certain parts of the brain rather than a whole body. Then they kill the vital neurons, or nerve cells, through which the brain does its primary work.

DR. SAM GANDY: Scientists sometimes describe these as resembling Brillo pads. You could see them building up outside nerve cells and in between nerve cells. These then would be supplying the poison that would kill this nerve cell.

SUSAN DENTZER: As the nerve cells die, their inner skeletons collapse, forming what are called tangles. Many scientists also think this process plays a pivotal role in Alzheimer's.

Using a plastic brain model, Gandy then showed us how all this damage starts in the brain's hippocampus region, which is responsible for memory and thought. That helps to explain a classic early Alzheimer's symptom: the loss of short-term memory, even as memories from long ago can somehow remain intact.

DR. SAM GANDY: As the disease progresses, it's on a malignant process. It destroys not only the nerve cells in the hippocampus responsible for memory, but many of the cells throughout the top of the brain, called the cortex. This is the master circuitry of the brain.

As the disease progresses, people become withdrawn from their environment, ultimately take to bed, and lose all ability to communicate with their environment or interact at all.

Developing new drugs

SUSAN DENTZER: In perhaps the disease's final insult, the part of the brain responsible for regulating basic body functions, like breathing, are not affected.

DR. SAM GANDY: This region here is called the brain stem.

SUSAN DENTZER: So even after having lost the ability to interact, patients like Gralnick can live a long time until an unrelated infection, like pneumonia, kills them.

Gandy says an effective treatment for Alzheimer's would block, reverse or at least slow down the formation of plaques and tangles. But current drugs on the market for treating Alzheimer's -- with names like Aricept, Exelon and Reminyl -- fall far short of that.

DR. SAM GANDY: They help the brain to compensate for a chemical deficiency that's present early in the disease. But as the disease progresses, their effect wears off and they become totally ineffective.

SUSAN DENTZER: So one goal now is to develop combinations of drugs that would work in various ways to attack the fundamental disease process.

That's the hope now of global pharmaceutical companies, which are exploring as many as 140 different compounds for that purpose. If successful, several could one day be used much like AIDS cocktails to hold Alzheimer's in check, or at least turn it from an inevitable slide downward into a more slowly progressing, chronic disease.

STEPHEN MCCONNELL: If science can produce a breakthrough that simply slows the progression of this disease and delays its onset just by a couple of years, it will save $50 billion a year in the Medicare program, a savings of $13 for every dollar spent on research.

SUSAN DENTZER: One pharmaceutical company working especially hard toward that goal is Wyeth, where Bob Essner is chairman and CEO. He says watching several friends and relatives suffer from the disease has made him impassioned on the subject.

ROBERT ESSNER, Chairman and CEO, Wyeth: What we're trying to do is to kind of put Alzheimer's disease now into the same priority that we've seen in the past with HIV-AIDS, with cancer, treatments for cancer, and most recently with avian flu.

SUSAN DENTZER: At the urging of Wyeth scientists, Essner agreed several years ago to plunge the company into a high-stakes, high-cost partnership with an Irish firm, Elan Pharmaceuticals.

Elan was working on a vaccine aimed at stimulating the body's immune system to make antibodies to destroy the amyloid plaques. Although the vaccine has been shown to work in mice, so far the human brain has proved far more complicated. In 2002, a clinical trial of the vaccine in patients with Alzheimer's was halted when it produced dangerous side effects.

Menelas Pangalos heads up neuroscience research at Wyeth.

MENELAS PANGALOS, Vice President for Neuroscience Research, Wyeth: There was basically an inflammation in the brains of these patients, and so the trial had to be stopped. But what was very exciting was that there were some hints that this drug was doing what it did in mice, in people.

A safer vaccine

SUSAN DENTZER: Wyeth is now helping Elan develop a potentially safer vaccine approach, as well as working on several other Alzheimer's-fighting drugs. And the company seems every bit as determined as Meryl Comer to raise awareness about the disease.

As a result, it provided seed money to form that organization she joined, ACT-AD. Essner says part of the goal is to persuade the U.S. Food and Drug Administration to find new ways to bring Alzheimer's therapies to patients as quickly as possible.

ROBERT ESSNER: If the FDA were to engage as a partner and give the same kind of priority they give to cancer drugs or HIV drugs, that they could move the process of development along faster and potentially get a cure available faster than they otherwise might.

SUSAN DENTZER: FDA officials told us the agency shares ACT-AD's goal of moving ahead as fast as possible on Alzheimer's. In a statement, the agency said, it is, quote, "actively working with manufacturers, medical researchers, and the Alzheimer's patient community to facilitate development of new and better products for patients."

The agency said a key priority is developing new ways to test the effectiveness of Alzheimer's drugs by using imaging devices, such as this one, to monitor subtle changes in the brains of patients.

Meanwhile, an even harder task for Alzheimer's advocates may be working to reverse cuts in the research budget for the disease at the National Institutes of Health. Congress cut the NIH's overall budget this year for the first time in 36 years, and President Bush has proposed no further increase for fiscal 2007; that would translate into $6 million less next year for Alzheimer's research.

DR. SAM GANDY: The outlook is incredibly grim. It's difficult now to encourage new, young investigators to enter this enterprise. And so, as the NIH budget goes down, these scientists, these professors, cannot be employed, and they go elsewhere.

SUSAN DENTZER: The NIH's Dr. Norka Ruiz Bravo told us the proposed cuts were unfortunate, but unless Congress reverses them, they're inevitable at a time when the NIH budget is being squeezed to meet other government priorities.

DR. NORKA RUIZ BRAVO, Deputy Director for Extramural Research, NIH: There's no question that Alzheimer's is a devastating disease. I think we can all recognize that. It is, however, a very tough budget environment for NIH. The tough budget environment is going to affect all diseases, and Alzheimer's is one of many that it's going to affect.

SUSAN DENTZER: Comer says that's intolerable at a time that progress is so essential.

MERYL COMER: We need it fast, sooner rather than later, because I am terrified just by the notion that our generation will end up looking like my husband.

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